Figure 2 Brain MRI features of 3 representatives patients with MS who experienced WNS after FTY withdrawal Brain MRI features of 3 representatives patients.

Slides:

Advertisements

Similar presentations

Figure 2 ERG amplitude reduction in the follow-up study

Advertisements

Figure 1 Box plot of the venous diameter in lesions

Figure 1 Regional changes in FA values

Figure 1 Brain MRI findings in the present case

Figure MRI of anti-MOG-IgG–associated myelitis

Figure 2 Evolution of MRI abnormalities in faciobrachial dystonic seizures Axial fluid- attenuated inversion recovery (FLAIR)-weighted images from patient.

Figure 2 Spinal cord lesions

Figure Neuroimaging and pathology

Figure 4 Correlation of age with [11C](R)-PK11195 binding in the normal-appearing white matter (NAWM) and thalami Correlation of age with [11C](R)-PK11195.

Figure 1 Coronal MRI images showing the evolution of white matter abnormality and atrophy of patient 1 Coronal MRI images showing the evolution of white.

Figure 2 Disease progression slowed during each round of Treg infusions and correlated with increased Treg suppressive function Disease progression slowed.

Figure Facial photograph during headache attack and brain and upper cervical cord MRI Facial photograph during headache attack and brain and upper cervical.

Figure 1 Treg percentage and suppressive function increased during each round of Treg infusions Treg percentage and suppressive function increased during.

Figure 1 Spine MRI, sagittal and axial views of patients with idiopathic transverse myelitis with VPS37A mutations Spine MRI, sagittal and axial views.

Figure 3 Example of venous narrowing

Figure Immune checkpoint inhibitor–induced encephalitis before and after treatment with natalizumab Immune checkpoint inhibitor–induced encephalitis before.

Figure 1 MRI head in faciobrachial dystonic seizures (A) Axial fluid-attenuated inversion recovery image from patient 3 in table 2 shows T2-weighted hyperintensity.

Figure 1 Histopathologic features of a chronic active and a chronic plaque in the MS brain Histopathologic features of a chronic active and a chronic plaque.

Figure 1. Prebiopsy and postbiopsy MRI

Figure 4 Detection of EBER+ cells in MS and control brains by in situ hybridization Detection of EBER+ cells in MS and control brains by in situ hybridization.

Figure 1 ERG peak time delay at baseline

Figure 1 Quantitative spinal cord MRI maps and segmentations

Figure 1 Cerebral MRI during the disease course Cerebral MRI with multiple cerebral supratentorial lesions during the disease course: periventricular lesions.

Figure 2 Correlation between total IgG levels and anti-AQP4 IgG titer

Figure 2 T2-weighted and subtraction images

Figure MRI and neuropathologic characteristics of the tumefactive demyelinating lesion in our patient MRI and neuropathologic characteristics of the tumefactive.

Figure 2 Facial appearance and brain imaging

Figure 1 White matter lesion central vein visibility in MS and absence in small vessel disease (SVD)‏ White matter lesion central vein visibility in MS.

Figure 2 Example of venous narrowing

Figure 1 MRI of inflammatory myelitis before and after treatment

Figure 1 Radiologic features of human myelin oligodendrocyte glycoprotein immunoglobulin G–positive patients with cranial nerve involvement Radiologic.

Figure 1 Illustration of white matter– and lesion-associated regions of interest (ROIs)‏ Illustration of white matter– and lesion-associated regions of.

Figure Family tree with the HLA haplotyping of 6 members of the family

Figure Fundoscopic examination of the VZV-infected left eye over time

Figure 2 Cerebral and spinal MRI (A) Restricted diffusion of both optic nerves (arrows) on diffusion-weighted and apparent diffusion coefficient imaging.

Figure Alluvial plot of modified Rankin Scale (mRS) scores during and at the end of hospital stay Alluvial plot of modified Rankin Scale (mRS) scores during.

Figure 1 MRI findings over time

Figure 2 Longitudinal relationship between CSF glucose and protein changes Longitudinal relationship between CSF glucose and protein changes Delta glucose.

Figure 1 Brain MRI Brain MRI (A) Axial fluid-attenuated inversion-recovery images show perilesional edema in both cerebellar hemisphere and hypointense.

Figure Brain MRI findings before and during appearance of lymphoproliferative disorder and pathology findings of cerebellar lesion Brain MRI findings before.

Figure 2 Global tau-PET distribution in familial prion disease mirrors the distribution seen in Alzheimer disease Global tau-PET distribution in familial.

Figure 2 Kaplan-Meier survival graphs for 10-year risks of overall and post-90-day recurrent ischemic stroke (IS) and death Kaplan-Meier survival graphs.

Figure 1 Stacked bar chart depicts the proportion of patients with diffusion-weighted imaging (DWI)+ and DWI− scans categorized by index event type TIA.

Figure 1 Annualized percentage brain volume change

Figure 2 BVL according to on-study disability worsening

Figure 2 Repopulation of CD19+ cells in low and high BSA patients and calculation of the BSA Repopulation of CD19+ cells in low and high BSA patients and.

Figure 2 Frequency of the proportion of total WMLs with central veins in PPMS, RRMS, and SVD Frequency of the proportion of total WMLs with central veins.

Figure Spinal cord imaging (A, B) Sagittal and axial T2-weighted cervical spine MRI demonstrating hyperintensities in the central gray matter of patient.

Yian Gu et al. Neurol Neuroimmunol Neuroinflamm 2019;6:e521

Ingo Kleiter et al. Neurol Neuroimmunol Neuroinflamm 2018;5:e504

Gitanjali Das et al. Neurol Neuroimmunol Neuroinflamm 2018;5:e453

Figure Serial brain MRI of the patient with encephalitis and spontaneous recovery accompanying IgLON5 autoimmunity Serial brain MRI of the patient with.

Figure 1 MRIs (case 1)‏ MRIs (case 1) An enlarging T2 lesion in the cerebral white matter near the angular gyrus and a new lesion in the left middle cerebellar.

Figure 2 MRIs (cases 2 and 3)‏

Figure 1 Imaging and histopathologic characteristics of patients with CNS-FHL Imaging and histopathologic characteristics of patients with CNS-FHL FLAIR.

Figure A 57-year-old man with relapsing-remitting MS (RRMS) and new-onset ataxia A 57-year-old man with relapsing-remitting MS (RRMS) and new-onset ataxia.

Figure 4 Patient 3 MRI evolution over time

Figure 3 Patient 2 MRI evolution over time before relapse

Figure 1 Segmentation of the normal-appearing periependymal white matter Segmentation of the normal-appearing periependymal white matter The figure demonstrates.

Figure 2 Time from incident ADS event to MS diagnosis

Figure 2 Patient 1 MRI evolution over time

Figure 2 Nonhuman primate brain immunohistochemistry

Figure 1 MRI of both patients with IgG4-HP and spinal cord arteriography of the first patient MRI of both patients with IgG4-HP and spinal cord arteriography.

Figure 4 Venn diagram for B-cell Sup proteins compared with proteins from exosome-enriched fractions from a human B-cell line Venn diagram for B-cell Sup.

Figure 3 A receiver operating characteristic curve of days to IVMP as a predictor of failure to regain 0.2 logMAR (20/30) vision (AUC 0.84, p < 0.001)‏

Figure 1 EDSS score (A), T2LV (B) and T1LV (C) courses in patients who experienced WNS after FTY withdrawal EDSS score (A), T2LV (B) and T1LV (C) courses.

Figure 2 Region of interest (ROI)-specific [11C](R)-PK11195 binding in patients with relapsing-remitting MS (RRMS), patients with secondary progressive.

Figure 1 Axial FLAIR brain MRI obtained on admission to the ICU demonstrated (A1) old hyperintense subcortical lesions (arrowhead), new superimposed on.

Figure (A and B) Effect of canakinumab in muscle strength measured in each patient as mean bilateral GF (A) and TMS (B) during the mean study period of.

Figure 1 MRIs MRIs (A and B) Axial FLAIR images of the brain demonstrate multifocal parenchymal lesions including the right hippocampus, right midbrain,

Presentation transcript:

Figure 2 Brain MRI features of 3 representatives patients with MS who experienced WNS after FTY withdrawal Brain MRI features of 3 representatives patients with MS who experienced WNS after FTY withdrawal (A) Tumefactive demyelination pattern (TDL), Pt.3. (A.a) Axial T2/FLAIR images, showing large and edematous lesions, causing mass effect on adjacent structures; (A.b) Axial TSE-T1 after Gd administration images, showing multiple ring and nodular enhancing lesions; (A.c) axial DWI (on the left) and correspondent ADC maps (on the right) images, showing hyperintense lesions on DWI with correspondent hypointense signal on ADC maps (red arrows), expression of restricted diffusion. (B) Punctuated pattern (PL), Pt.1, SPMS patient. (B.a) axial TSE-T2 images, medium in size (already detectable in previous scans) and new small hyperintense lesions, with no edema and mass effect; (B.b) axial TSE-T1 after gadolinium administration images, showing innumerable millimetric enhancing lesions, both in infratentorial and supratentorial areas. (B.c) axial DWI (on the left) and correspondent ADC maps (on the right) images, showing hyperintense lesions on DWI with correspondent hypointense signal on ADC maps (red arrows), expression of restricted diffusion. (C) Classic MS pattern (CL). (Pt.6) (C.a) Axial FLAIR images, showing medium in size lesions, with no edema and mass effect; (B.b) axial TSE-T1 after gadolinium administration images, showing nodular and ring enhancing lesions. (C.c) Axial DWI (on the left) and correspondent ADC maps (on the right) images, showing hyperintense lesions on DWI with correspondent hyperintense signal on ADC maps (“T2-shine through effect”). Caterina Lapucci et al. Neurol Neuroimmunol Neuroinflamm 2019;6:e566 Copyright © 2019 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of the American Academy of Neurology.